CA-2+-FATTY ACID INTERACTION IN THE CONTROL OF HEPATIC GLUCONEOGENESIS

被引:8
作者
GONZALEZMANCHON, C [1 ]
MENAYA, J [1 ]
AYUSO, MS [1 ]
PARRILLA, R [1 ]
机构
[1] CSIC,CTR INVEST BIOL,ENDOCRINE PHYSIOL UNIT,VELAZQUEZ 144,E-28006 MADRID,SPAIN
关键词
(Rat liver); Calcium ion-fatty acid interaction; Fatty acid; Gluconeogenesis;
D O I
10.1016/0167-4889(90)90125-W
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Calcium depletion induced by perfusing livers with calcium-free buffer did not alter the rates of basal glucose production from pyruvate or from increasing concentrations of lactate. However, calcium deficiency selectively prevented the fatty acid-induced stimulation of gluconeogenesis from lactate. This effect is not related to the higher NAD redox potential consistently observed in Ca2+-deficient livers. On the other hand, octanoate was capable of inducing dose-dependent changes in the [pyruvate]0.5 in calcium-depleted livers perfused with lactate, ruling out that low cellular calcium content could perturb the mitochondrial transport of pyruvate. The observation that the effect of calcium deficiency can be overcome by supraphysiological concentrations of pyruvate supports the proposal that stimulation of the maximal capacity of the gluconeogenic pathway by fatty acid relies largely on the tricarboxylic acid cycle activity, restricted in calcium deficiency conditions. © 1990.
引用
收藏
页码:215 / 220
页数:6
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